Monday, July 2, 2018

Ketamine Is Good At Treating Depression And Here’s How We Think It Works

As more and more evidence demonstrating that ketamine, a veterinary anesthetic used recreationally by many people, can actually produce benefits, scientists are increasingly looking at the possibility that ketamine can be used to treat disorders like depression.

Many casual ketamine users have long known that ketamine can alleviate depression, or at least the symptoms of it. But a hesitance in the scientific community to listen to non-PhDs and a barbaric drug war have long prevented adequate research into the subject.

The research that has been done, however, has discovered that recreational users were right. Now scientists are trying to figure out how ketamine actually alleviates the symptoms of depression.

In a new study entitled, “NMDAR-Independent, cAMP-dependent antidepressant actions of ketamine,” published in the Nature journal Molecular Psychiatry.

Researchers from the University of Illinois at Chicago looked at the mechanism of how ketamine dampens the symptoms of depression. These researchers claim that ketamine works similar to SSRIs. Essentially, the main active component is the G protein, which produces cyclic AMP, a messenger that nerve cells need in order to signal properly.

Earlier research has shown that people with depression have higher numbers of G proteins in their cell membranes. Researchers believe that this dampens the signals of cells which then contributes to the symptoms of depression, particularly the feeling of emotional numbness.

SSRIs claim to help move G proteins off of lipid rafts on the cell membrane which allows them to work freely again. This is what ketamine appears to do, but the difference is that it does so within 15 minutes.

Even more so, the G proteins seem very sluggish when they move back on to the lipid rafts, which might explain ketamine’s long lasting effect on the symptoms of depression.

This brings into question what some previous scientists believe made ketamine work which they theorize was the blocking of the NMDA receptor.

Mark Rasenick, distinguished professor of physiology and psychiatry at UIC College of Medicine said:

When G proteins move out of the lipid rafts, it allows for better communication among brain cellss, which is known to help alleviate some of the symptoms of depression.

This further illustrates that the movement of G proteins out of lipid rafts is a true biomarker of the efficacy of antidepressants, regardless of how they work. It confirms that our cell model is a useful tool for showing the effect of potential new antidepressant drug candidates on the movement of G proteins and the possible efficacy of these drugs in treating depression.

Clearly more research needs to be done since approaching depression as a chemical imbalance alone has long been called into question. However, chemical interplay can definitively play a role as well. This research is yet another example of why constructing a massive police state and prison complex in which to place people who chose to consume substances for whatever reason is not only bad economics and bad for mental health, it’s actually tragic.

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